Toxicological Sciences Publishes EPHD Scientists’ Manuscript

Eight members of NHEERL’s Environmental Public Health Division (EPHD), along with a researcher from the laboratory’s Research Cores Unit and an interim National Program Director, co-authored a paper (see description below) that was published early this month by Toxicological Sciences.

Diesel exhaust (DE) is a major contributor to traffic-related fine particulate matter (PM2.5). Although inroads have been made in understanding the mechanisms of PM-related health effects, DE's complex mixture of PM, gases, and volatile organics makes it difficult to determine how the constituents contribute to DE's effects. We hypothesized that exposure to particle-filtered DE (gases alone) will elicit less cardiac effects than whole DE (particles plus gases). In addition, we hypothesized that spontaneously hypertensive rats (SHRs) will be more sensitive to the electrocardiographic effects of DE exposure than Wistar Kyoto rats (WKY; background strain with normal blood pressure). SHRs and WKY rats, implanted with telemeters to monitor electrocardiogram and heart rate (HR), were exposed once for 4 h to 150 ug/m3 or 500 ug/m3 of whole (wDE; gases plus PM) or filtered (fDE; gases alone) DE or filtered air. Exposure to fDE, but not wDE, caused immediate electrocardiographic alterations in cardiac repolarization (ST depression) and atrioventricular conduction block (PR prolongation), as well as bradycardia in SHRs. Exposure to wDE, but not fDE, caused postexposure ST depression and increased sensitivity to the pulmonary C fiber agonist capsaicin in SHRs. The only notable effect of DE exposure in WKY rats was a decrease in HR. Taken together, hypertension may predispose to the potential cardiac effects of DE, and components of DE may have divergent effects with some eliciting immediate irritant effects (e.g., gases), whereas others (e.g., PM) trigger delayed effects potentially via separate mechanisms.